However, the most striking results obtained were that the D I DA receptor antagonist SCH 23390 exhibited an extremely high potency and efficacy in reducing sleep latency, a significant effect being observed with 3 ~g/kg (Fratta et al., 1987; Table 1). Vice versa, the administration of the D 2 DA receptor agonist quinpirole produced a biphasic effect. Doses of quinpirole small enough (10-50 /xg/kg) to selectively activate DA autoreceptors reduced sleep latency, while 'postsynaptic' doses (above 200/xg/kg) prolonged sleep latency at the highest doses (Fig. 1). Also the administration of the specific D 1 DA receptor agonist SKF 38393 markedly prolonged the period of insomnia with the correlated behaviora